Respiratory Acidosis as a Diagnostic Clue in Symptomatic Epilepsy With Stroke Mimics: A Case Report.

Stroke mimics are difficult to differentiate from each other. Symptomatic epilepsy can also occur, but it is necessary to perform a magnetic resonance imaging (MRI) scan to distinguish it from a stroke. Although respiratory acidosis has been reported to occur with partial-onset seizures due to prolonged apnea, respiratory acidosis is rarely suspected to be a sign of epilepsy. We report a case in which respiratory acidosis helped to diagnose symptomatic epilepsy with stroke mimics. The patient was a 52-year-old female who was brought to the emergency room with the chief complaint of difficulty in talking. When she visited the hospital, sensory aphasia was observed, and a computed tomography (CT) scan was performed. She vomited after the CT scan, and an arterial blood gas analysis showed a pH of 7.26 with a PaCO2 level of 71 mmHg, indicating respiratory acidosis. After the administration of diazepam, the seizures abated and her sensory aphasia improved. Later, an investigation of the patient's history revealed symptomatic epilepsy and discontinuation of antiepileptic drugs. If unexplained respiratory acidosis is noted in a patient with stroke mimics, a further investigation of the patient's history and physical examination may help to diagnose symptomatic epilepsy.

Standard vs. carbone dioxide adapted kidney replacement therapy in hypercapnic ARDS patients: a randomized controlled pilot trial (BigBIC).

BACKGROUND: Current continuous kidney replacement therapy (CKRT) protocols ignore physiological renal compensation for hypercapnia. This study aimed to explore feasibility, safety, and clinical benefits of pCO2-adapted CKRT for hypercapnic acute respiratory distress syndrome (ARDS) patients with indication for CKRT. METHODS: We enrolled mechanically ventilated hypercapnic ARDS patients (pCO2 > 7.33 kPa) receiving regional citrate anticoagulation (RCA) based CKRT in a prospective, randomized-controlled pilot-study across five intensive care units at the Charité-Universitätsmedizin Berlin, Germany. Patients were randomly assigned 1:1 to the control group with bicarbonate targeted to 24 mmol/l or pCO2-adapted-CKRT with target bicarbonate corresponding to physiological renal compensation. Study duration was six days. Primary outcome was bicarbonate after 72 h. Secondary endpoints included safety and clinical endpoints. Endpoints were assessed in all patients receiving treatment. RESULTS: From September 2021 to May 2023 40 patients (80% male) were enrolled. 19 patients were randomized to the control group, 21 patients were randomized to pCO2-adapted-CKRT. Five patients were excluded before receiving treatment: three in the control group (consent withdrawal, lack of inclusion criteria fulfillment (n = 2)) and two in the intervention group (lack of inclusion criteria fulfillment, sudden unexpected death) and were therefore not included in the analysis. Median plasma bicarbonate 72 h after randomization was significantly higher in the intervention group (30.70 mmol/l (IQR 29.48; 31.93)) than in the control group (26.40 mmol/l (IQR 25.63; 26.88); p < 0.0001). More patients in the intervention group received lung protective ventilation defined as tidal volume < 8 ml/kg predicted body weight. Thirty-day mortality was 10/16 (63%) in the control group vs. 8/19 (42%) in the intervention group (p = 0.26). CONCLUSION: Tailoring CKRT to physiological renal compensation of respiratory acidosis appears feasible and safe with the potential to improve patient care in hypercapnic ARDS. TRIAL REGISTRATION: The trial was registered in the German Clinical Trials Register (DRKS00026177) on September 9, 2021 and is now closed.

Impact of AKI on metabolic compensation for respiratory acidosis in ICU patients with AECOPD.

PURPOSE: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) can result in severe respiratory acidosis. Metabolic compensation is primarily achieved by renal retention of bicarbonate. The extent to which acute kidney injury (AKI) impairs the kidney's capacity to compensate for respiratory acidosis remains unclear. MATERIALS AND METHODS: This retrospective analysis covers clinical data between January 2009 and December 2021 for 498 ICU patients with AECOPD and need for respiratory support. RESULTS: 278 patients (55.8%) presented with or developed AKI. Patients with AKI exhibited higher 30-day-mortality rates (14.5% vs. 4.5% p = 0.001), longer duration of mechanical ventilation (median 90 h vs. 14 h; p = 0.001) and more severe hypercapnic acidosis (pH 7.23 vs. 7.28; pCO2 68.5 mmHg vs. 61.8 mmHg). Patients with higher AKI stages exhibited lower HCO3-/pCO2 ratios and did not reach expected HCO3- levels. In a mixed model analysis with random intercept per patient we analyzed the association of pCO2 (independent) and HCO3- (dependent variable). Lower estimates for averaged change in HCO3- were observed in patients with more severe AKI. CONCLUSION: AKI leads to poor outcomes and compromises metabolic compensation of respiratory acidosis in ICU patients with AECOPD. While buffering agents may aid compensation for severe AKI, their use should be approached with caution.

Seizure control via pH manipulation: a phase II double-blind randomised controlled trial of inhaled carbogen as adjunctive treatment of paediatric convulsive status epilepticus (Carbogen for Status Epilepticus in Children Trial (CRESCENT)).

BACKGROUND: Paediatric convulsive status epilepticus is the most common neurological emergency presenting to emergency departments. Risks of resultant neurological morbidity and mortality increase with seizure duration. If the seizure fails to stop within defined time-windows, standard care follows an algorithm of stepwise escalation to more intensive treatments, ultimately resorting to induction of general anaesthesia and ventilation. Additionally, ventilatory support may also be required to treat respiratory depression, a common unwanted effect of treatment. There is strong pre-clinical evidence that pH (acid-base balance) is an important determinant of seizure commencement and cessation, with seizures tending to start under alkaline conditions and terminate under acidic conditions. These mechanisms may be particularly important in febrile status epilepticus: prolonged fever-related seizures which predominantly affect very young children. This trial will assess whether imposition of mild respiratory acidosis by manipulation of inhaled medical gas improves response rates to first-line medical treatment. METHODS: A double-blind, placebo-controlled trial of pH manipulation as an adjunct to standard medical treatment of convulsive status epilepticus in children. The control arm receives standard medical management whilst inhaling 100% oxygen; the active arm receives standard medical management whilst inhaling a commercially available mixture of 95% oxygen, 5% carbon dioxide known as 'carbogen'. Due to the urgent need to treat the seizure, deferred consent is used. The primary outcome is success of first-line treatment in seizure cessation. Planned subgroup analyses will be undertaken for febrile and non-febrile seizures. Secondary outcomes include rates of induction of general anaesthesia, admission to intensive care, adverse events, and 30-day mortality. DISCUSSION: If safe and effective 95% oxygen, 5% carbon dioxide may be an important adjunct in the management of convulsive status epilepticus with potential for pre-hospital use by paramedics, families, and school staff. TRIAL REGISTRATION: EudraCT: 2021-005367-49. CTA: 17136/0300/001. ISRCTN: 52731862. Registered on July 2022.

Acute sodium bicarbonate administration improves ventilatory efficiency in experimental respiratory acidosis: clinical implications.

Administering sodium bicarbonate (NaHCO3) to patients with respiratory acidosis breathing spontaneously is contraindicated because it increases carbon dioxide load and depresses pulmonary ventilation. Nonetheless, several studies have reported salutary effects of NaHCO3 in patients with respiratory acidosis but the underlying mechanism remains uncertain. Considering that such reports have been ignored, we examined the ventilatory response of unanesthetized dogs with respiratory acidosis to hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) and compared it with that of animals with normal acid-base status or one of the remaining acid-base disorders. Ventilatory response to NaHCO3 infusion was evaluated by examining the ensuing change in PaCO2 and the linear regression of the PaCO2 vs. pH relationship. Strikingly, PaCO2 failed to increase and the ΔPaCO2 vs. ΔpH slope was negative in respiratory acidosis, whereas PaCO2 increased consistently and the ΔPaCO2 vs. ΔpH slope was positive in the remaining study groups. These results cannot be explained by differences in buffering-induced decomposition of infused bicarbonate or baseline levels of blood pH, PaCO2, and pulmonary ventilation. We propose that NaHCO3 infusion improved the ventilatory efficiency of animals with respiratory acidosis, i.e., it decreased their ratio of total pulmonary ventilation to carbon dioxide excretion (VE/VCO2). Such exclusive effect of NaHCO3 infusion in animals with respiratory acidosis might emanate from baseline increased VD/VT (dead space/tidal volume) caused by bronchoconstriction and likely reduced pulmonary blood flow, defects that are reversed by alkali infusion. Our observations might explain the beneficial effects of NaHCO3 reported in patients with acute respiratory acidosis.

Extracorporeal membrane oxygenation treatment for severe asthma had unexpected adverse effects: a case report.

Asthma, a chronic respiratory ailment, affects millions worldwide. Extracorporeal membrane oxygenation (ECMO) has gained traction as a life-saving intervention for patients with severe asthma who are unresponsive to conventional treatments. However, complications associated with ECMO, including electrolyte imbalances and hemorrhage, can have significant clinical implications. This case report highlights a 49 years-old male patient with severe asthma who developed pronounced hypokalemia and hemorrhage following venovenous ECMO (VVECMO) therapy. Despite potassium supplementation, serum potassium levels continued declining before normalizing after 24 h. The patient subsequently experienced gastrointestinal bleeding, cerebral hemorrhage, and extensive cerebral infarction, ultimately resulting in a deep coma. Hypokalemia during ECMO therapy can result from a rapid reduction of carbon dioxide, ß-receptor agonist use, corticosteroid use, and diuretic administration. Hemorrhage is another common ECMO complication, often linked to heparin anticoagulation therapy. Clinicians should be aware of potential complications and adopt appropriate prevention and management strategies when using ECMO in patients with severe asthma.

Hypercapnia in hospitalized children and adolescents with anorexia nervosa as a predictive marker for readmission: a prospective study.

PURPOSE: To determine whether hypercapnia is associated with risk of hospital readmission related to anorexia nervosa (AN) in children and adolescents. METHODS: We performed a prospective study of patients ≤ 18 years old admitted due to AN decompensation from November 2018 to October 2019. Both subtypes of AN, restricting subtype (AN-R) and binge-eating/purging subtype (AN-BP), were included. Study participants were evaluated upon admission, at discharge and six months after discharge. T-tests or Mann-Whitney U tests was used to compare means values. Pearson or Spearman correlations were used to measure the association between two variables. Logistic regression models were developed to evaluate the relationship between scoring methods and readmission. RESULTS: Of the 154 persons admitted during the study period, 131 met the inclusion criteria. Median age was 15.1 years. At admission, 71% of participants were malnourished and 33 (25%) had been previously admitted. We observed a marked decrease in venous pH and stable pCO2 elevation during follow-up period. Hypercapnia at discharge was associated with a twofold increased likelihood of readmission and the odds of readmission increased as discharge pCO2 rose. These findings did not depend on AN subtype or participant sex. Electrolytes persisted within the normal range. CONCLUSION: Hypercapnia and respiratory acidosis are common alterations in children and adolescents hospitalized due to AN decompensation. Hypercapnia persists for at least 6 months after discharge despite clinical improvement and is associated with higher odds of readmission. This is the first study to identify an abnormal laboratory finding as a potential predictor of readmission in AN. LEVEL OF EVIDENCE: IV: Multiple time series without intervention.

Causes of hypercapnic respiratory failure: a population-based case-control study.

OBJECTIVE: There are no population-based data on the relative importance of specific causes of hypercapnic respiratory failure (HRF). We sought to quantify the associations between hospitalisation with HRF and potential antecedent causes including chronic obstructive pulmonary disease (COPD), obstructive sleep apnea, and congestive cardiac failure. We used data on the prevalence of these conditions to estimate the population attributable fraction for each cause. METHODS: A case-control study was conducted among residents aged ≥ 40 years from the Liverpool local government area in Sydney, Australia. Cases were identified from hospital records based on PaCO2 > 45 mmHg. Controls were randomly selected from the study population using a cluster sampling design. We collected self-reported data on medication use and performed spirometry, limited-channel sleep studies, venous sampling for N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, and sniff nasal inspiratory pressure (SNIP) measurements. Logistic regression analyses were performed using directed acyclic graphs to identify covariates. RESULTS: We recruited 42 cases and 105 controls. HRF was strongly associated with post-bronchodilator airflow obstruction, elevated NT-proBNP levels, reduced SNIP measurements and self-reported opioid medication use. There were no differences in the apnoea-hypopnea index or oxygen desaturation index between groups. COPD had the highest population attributable fraction (42%, 95% confidence interval 18% to 59%). CONCLUSIONS: COPD, congestive cardiac failure, and self-reported use of opioid medications, but not obstructive sleep apnea, are important causes of HRF among adults over 40 years old. No single cause accounts for the majority of cases based on the population attributable fraction.

Respiratory Acid-Base Disorders.

Respiratory acid-base disorders are often not thought of as frequently as their metabolic cousins, which occur more frequently in the emergency department. Although most respiratory and acid-base disturbances are driven by lung pathology, central nervous system and other organ systems can and do play a role as well. Although managing the airway and appropriate mechanical ventilation may be necessary, it is akin to placing a band-aid on a large wound. It is crucial for the emergency clinician to discover the etiology of the disturbance as management depends on treating the underlying etiology to prevent worsening acid-base status.

Evaluation of the safety and efficacy of extracorporeal carbon dioxide removal in the critically ill using the PrismaLung+ device.

BACKGROUND: Several extracorporeal carbon dioxide removal (ECCO2R) devices are currently in use with variable efficacy and safety profiles. PrismaLung+ is an ECCO2R device that was recently introduced into clinical practice. It is a minimally invasive, low flow device that provides partial respiratory support with or without renal replacement therapy. Our aim was to describe the clinical characteristics, efficacy, and safety of PrismaLung+ in patients with acute hypercapnic respiratory failure. METHODS: All adult patients who required ECCO2R with PrismaLung+ for hypercapnic respiratory failure in our intensive care unit (ICU) during a 6-month period between March and September 2022 were included. RESULTS: Ten patients were included. The median age was 55.5 (IQR 41-68) years, with 8 (80%) male patients. Six patients had acute respiratory distress syndrome (ARDS), and two patients each had exacerbations of asthma and chronic obstructive pulmonary disease (COPD). All patients were receiving invasive mechanical ventilation at the time of initiation of ECCO2R. The median duration of ECCO2R was 71 h (IQR 57-219). A significant improvement in pH and PaCO2 was noted within 30 min of initiation of ECCO2R. Nine patients (90%) survived to weaning of ECCO2R, eight (80%) survived to ICU discharge and seven (70%) survived to hospital discharge. The median duration of ICU and hospital stays were 14.5 (IQR 8-30) and 17 (IQR 11-38) days, respectively. There were no patient-related complications with the use of ECCO2R. A total of 18 circuits were used in ten patients (median 2 per patient; IQR 1-2). Circuit thrombosis was noted in five circuits (28%) prior to reaching the expected circuit life with no adverse clinical consequences. CONCLUSION(S): PrismaLung+ rapidly improved PaCO2 and pH with a good clinical safety profile. Circuit thrombosis was the only complication. This data provides insight into the safety and efficacy of PrismaLung+ that could be useful for centres aspiring to introduce ECCO2R into their clinical practice.

The Absence of an Na+/Ca2+Exchanger (NCX) in Bullfrog Proximal Tubules and Cellular pH is More Influential Than Cellular Ca2+ on Proximal Na Transport.

BACKGROUND/AIMS: The functional significance of the Na+/Ca2+ exchanger (NCX) in basolateral membranes in the proximal tubule remains controversial. The key factor in crosstalk between the apical and basolateral sides is not known. METHODS: We investigated the basolateral membranes, using double-barreled Ca2+ or pH ion-selective microelectrodes. We used doubly perfused bullfrog kidneys in vivo, and switched the basolateral solution (renal portal vein) to experimental solutions. RESULTS: In the control, cellular pH (pHi) was 7.33 ± 0.032 (mean ± SE, n = 7) and in separate experiments, cellular Ca2+ activity (aCai) was 249.6 ± 35.54 nM (n = 28). Changing to respiratory acidosis, pHi was significantly acidified by 0.123 pH units on average and the change of aCai was +53.1 nM (n = 9 ns). In metabolic acidosis, pHi was reduced by 0.151 while aCai was reduced by 143.4. Using the 30 mM K+ solution, pHi was increased by 0.233 while aCai was reduced by 203.9, with depolarization. Both ionomycin and ouabain caused aCai to increase. In the 0.5 mM Na+ solution (replaced with BIDAC Cl), pHi was reduced by 0.177. No changes in aCai (+49.8 ns) were observed although we recorded depolarization of 15.2 mV. In the 0.5 mM Na+ solution, replaced with raffinose, no changes in aCai (-126.4 ns) were observed with depolarization (6.5 ns). CONCLUSION: Our results suggest that thermodynamic calculations of cellular Na+ concentration led to the conclusion that either a Na+/HCO3- exchanger (NBC) or NCX could be present in the same basolateral membrane. H+ ions are the most plausible key factor in the crosstalk.

Respiratory Acidosis and Respiratory Alkalosis: Core Curriculum 2023.

The respiratory system plays an integral part in maintaining acid-base homeostasis. Normal ventilation participates in the maintenance of an open buffer system, allowing for excretion of CO2 produced from the interaction of nonvolatile acids and bicarbonate. Quantitatively of much greater importance is the excretion of CO2 derived from volatile acids produced from the complete oxidation of fat and carbohydrate. A primary increase in CO2 tension of body fluids is the cause of respiratory acidosis and develops most commonly from one or more of the following: (1) disorders affecting gas exchange across the pulmonary capillary, (2) disorders of the chest wall and the respiratory muscles, and/or (3) inhibition of the medullary respiratory center. Respiratory alkalosis or primary hypocapnia is most commonly caused by disorders that increase alveolar ventilation and is defined by an arterial partial pressure of CO2 <35 mm Hg with subsequent alkalization of body fluids. Both disorders can lead to life-threatening complications, making it of paramount importance for the clinician to have a thorough understanding of the cause and treatment of these acid-base disturbances.

Arterial oxygenation and acid-base status before and during oxygen supplementation in captive European bison (Bison bonasus) immobilized with etorphine-acepromazine-xylazine.

Chemical immobilization of captive European bison (Bison bonasus) is often required for veterinary care, transportation, or husbandry practices playing an important role in conservation breeding and reintroduction of the species. We evaluated the efficiency and physiological effects of an etorphine-acepromazine-xylazine combination with supplemental oxygen in 39 captive European bison. Animals were darted with a combination of 1.4 mg of etorphine, 4.5 mg of acepromazine, and 20 mg of xylazine per 100 kg based on estimated body mass. Arterial blood was sampled on average 20 min after recumbency and again 19 min later and analyzed immediately with a portable i-STAT analyzer. Simultaneously, heart rate, respiratory rate, and rectal temperature were recorded. Intranasal oxygen was started after the first sampling at a flow rate of 10 mL.kg-1.min-1 of estimated body mass until the end of the procedure. The initial mean partial pressure of oxygen (PaO2) was 49.7 mmHg with 32 out of 35 sampled bison presenting with hypoxemia. We observed decreased respiratory rates and pH and mild hypercapnia consistent with a mild respiratory acidosis. After oxygen supplementation hypoxemia was resolved in 21 out of 32 bison, but respiratory acidosis was accentuated. Bison immobilized with a lower initial drug dose required supplementary injections during the procedure. We observed that lower mean rectal temperatures during the immobilization event were significantly associated with longer recovery times. For three bison, minor regurgitation was documented. No mortality or morbidity related to the immobilizations were reported for at least 2 months following the procedure. Based on our findings, we recommend a dose of 0.015 mg.kg-1 etorphine, 0.049 mg.kg-1 acepromazine, and 0.22 mg.kg-1 xylazine. This dose reduced the need for supplemental injections to obtain a sufficient level of immobilization for routine management and husbandry procedures in captive European bison. Nevertheless, this drug combination is associated with development of marked hypoxemia, mild respiratory acidosis, and a small risk of regurgitation. Oxygen supplementation is strongly recommended when using this protocol.

Increased Longevity of a Novel Gas Exchanger System for Low-Flow Veno-Venous Extracorporeal CO2 Removal in Acute Hypercapnic Respiratory Failure.

INTRODUCTION: Low-flow veno-venous extracorporeal CO2 removal (ECCO2R) is an adjunctive therapy to support lung protective ventilation or maintain spontaneous breathing in hypercapnic respiratory failure. Low-flow ECCO2R is less invasive compared to higher flow systems, while potentially compromising efficiency and membrane lifetime. To counteract this shortcoming, a high-longevity system has recently been developed. Our hypotheses were that the novel membrane system provides runtimes up to 120 h, and CO2 removal remains constant throughout membrane system lifetime. METHODS: Seventy patients with pH ≤ 7.25 and/or PaCO2 ≥9 kPa exceeding lung protective ventilation limits, or experiencing respiratory exhaustion during spontaneous breathing, were treated with the high-longevity ProLUNG system or in a control group using the original gas exchanger. Treatment parameters, gas exchanger runtime, and sweep-gas VCO2 were recorded across 9,806 treatment-hours and retrospectively analyzed. RESULTS: 25/33 and 23/37 patients were mechanically ventilated as opposed to awake spontaneously breathing in both groups. The high-longevity system increased gas exchanger runtime from 29 ± 16 to 48 ± 36 h in ventilated and from 22 ± 14 to 31 ± 31 h in awake patients (p < 0.0001), with longer runtime in the former (p < 0.01). VCO2 remained constant at 86 ± 34 mL/min (p = 0.11). Overall, PaCO2 decreased from 9.1 ± 2.0 to 7.9 ± 1.9 kPa within 1 h (p < 0.001). Tidal volume could be maintained at 5.4 ± 1.8 versus 5.7 ± 2.2 mL/kg at 120 h (p = 0.60), and peak airway pressure could be reduced from 31.1 ± 5.1 to 27.5 ± 6.8 mbar (p < 0.01). CONCLUSION: Using a high-longevity gas exchanger system, membrane lifetime in low-flow ECCO2R could be extended in comparison to previous systems but remained below 120 h, especially in spontaneously breathing patients. Extracorporeal VCO2 remained constant throughout gas exchanger system runtime and was consistent with removal of approximately 50% of expected CO2 production, enabling lung protective ventilation despite hypercapnic respiratory failure.

Lethal toxicity induced by combined ingestion of dietary acetic acid and carbamazepine.

Acetic acid is an organic acid that can be used in the food industry, which normally has an insignificant rate of adverse reactions when used rationally. However, irrational use can cause serious toxic effects and even death. In this context, the case of a death of a 52-year-old woman, involving the suspected voluntary use of food acetic acid, is presented, while toxicological and histopathological aspects were addressed for death mechanism elucidation. In this case, the pH value of 6.75 in blood, has shown severe metabolic acidosis after the ingestion of the large quantity of dietary acetic acid - about a liter. Also, the victim suffers from mental illness, carbamazepine being one of the treatment drugs. Liver damage, demonstrated by histopathological examination may be a consequence of both massive accumulation of carbamazepine in the liver and toxicity of food acetic acid. In conclusion, the hepatotoxicity induced by high level of carbamazepine was suspected of increasing the risk of multiple organ failure, in the context of acetic acid acute toxicity, highlighting the particularities of the case.

Single-institution experience of extracorporeal membrane oxygenation for near-fatal asthma.

Near-fatal asthma (NFA) is the most severe presentation of asthma. It is characterized by hypoxemic and hypercapnic respiratory failure requiring ventilatory assistance, including non-invasive ventilation and mechanical ventilation. However, NFA has a high mortality rate despite conventional therapy. Extracorporeal membrane oxygenation (ECMO) is a treatment modality that is increasingly being utilized as rescue therapy in patients with NFA that is refractory to mechanical ventilation. Prior analyses of the international Extracorporeal Life Support Organization (ELSO) registry data showed a survival rate of over 83% in patients placed on venovenous (VV) ECMO for NFA, but with notable rate of hemorrhagic complications. We report seven cases of adults with NFA requiring ECMO support at our large quaternary care institution between the years 2019 and 2022. All seven patients presented with respiratory failure in the setting of asthma exacerbation that progressed despite standard pharmacotherapy and mechanical ventilation. All patients survived to hospital discharge after ECMO support without hemorrhagic complications, highlighting the effectiveness and safety of ECMO when appropriately used in this population.

Sodium bicarbonate buffer for weaning from venovenous extracorporeal membrane oxygenation in patients with hypercapnic respiratory failure and acute renal failure.

Although the routine use of alkali buffer is not recommended in patients with respiratory acidosis, some patients may benefit from its administration. A 42-year-old man was treated with venovenous extracorporeal membrane oxygenation (VV-ECMO) and continuous venovenous hemodiafiltration (CVVHDF) due to necrotizing pneumonia and emphysematous cystitis with Klebsiella pneumoniae. Although the sweep gas flow rate of the VV-ECMO was gradually reduced, he failed to wean off VV-ECMO due to respiratory acidosis, followed by tachycardia and tachypnea on the 63rd day of VV-ECMO. Therefore, we mixed sodium bicarbonate in the replacement fluid of CVVHDF for 5 days to avoid an intolerable decrease in blood pH after discontinuing the VV-ECMO sweep gas. When the serum bicarbonate concentration was >30 mmol/L and pH was maintained at >7.30 with a PCO2 of >60 mmHg, VV-ECMO was finally decannulated. Sodium bicarbonate buffer through the replacement of CVVHDF fluid facilitated VV-ECMO weaning in a patient with hypercapnic respiratory failure.